About Me

My mother was murdered by what I call corporate and political homicide i.e. FOR PROFIT! she died from a rare phenotype of CJD i.e. the Heidenhain Variant of Creutzfeldt Jakob Disease i.e. sporadic, simply meaning from unknown route and source. I have simply been trying to validate her death DOD 12/14/97 with the truth. There is a route, and there is a source. There are many here in the USA. WE must make CJD and all human TSE, of all age groups 'reportable' Nationally and Internationally, with a written CJD questionnaire asking real questions pertaining to route and source of this agent. Friendly fire has the potential to play a huge role in the continued transmission of this agent via the medical, dental, and surgical arena. We must not flounder any longer. ...TSS

USDA’s announcement last week that a fourth case of bovine spongiform
encephalopathy (BSE) has been identified in the United States, in a dairy cow in
Central California, is a warning flag that current safeguards against BSE are
not adequate and USDA should take additional steps to protect the health of
animals and of the beef-eating public.

Consumers Union, the policy and advocacy arm of Consumer Reports, is
concerned that if additional steps are not taken now, this deadly disease could
circulate and amplify within US cattle. USDA should conduct a full and complete
investigation of this case, expand its surveillance program, and allow private
companies to test as well. USDA should conduct a full and complete investigation
of this new BSE case. USDA has confirmed to reporters that this case is an
“L-type” atypical strain of BSE.1 USDA therefore must be especially vigilant,
because this may well not be a “spontaneous” case, but rather may well have been
infected through feed, and may be particularly infectious in humans.

The L-type BSE strain has previously been identified in cattle in Europe2
and in Canada.3 This would suggest that the current case may have been
contracted through feed, rather than be a new spontaneous occurrence.

Studies further suggest that the L-type BSE can infect humans, possibly
even more easily than “classical” BSE. A study using humanized mice (mice
genetically engineered to

have brain prions like humans) suggested that L-type BSE could infect
humans.4 Another study showed oral transmission to a primate.5 The mouse study
also found shorter incubation periods than for classical BSE, making it a more
“virulent” strain.6 The fact that L-type BSE has been found before in cattle
makes it extremely important that USDA conduct a thorough and complete
investigation of this case. Not just all offspring, but all cows that consumed
the same feed as this cow, should be tested for BSE.

USDA should significantly increase its surveillance for BSE.

Given the very small size of the current USDA surveillance program, it
cannot be said with certainty whether this new case is an isolated one, or
whether it is indicative of a much larger problem.

USDA tests approximately 40,000 dead or slaughtered cattle annually for
BSE, only about .1 percent of the 35 million cattle slaughtered annually in the
United States. This is far too small a sample to provide the nation with the
assurance that our food supply is safe. In Europe and Japan, every animal over a
certain age is tested at slaughter. In the U.S., having recently found one case
of BSE in a program of just 40,000 tests annually, consumers need to know what
the results would be from a larger test program in order to maintain their
confidence in the U.S. beef supply.

Ideally USDA should test all cattle at slaughter over the age of 20 months
for several years. At a minimum, USDA should test at least 350,000 annually, for
at least three years, including all cows showing nervous system abnormalities,
downers, and a random selection of cattle slaughtered at more than 30 months of
age and cows sent to the renderers.

USDA should end its prohibition on private sector testing for BSE.

To augment USDA testing, and to assure meat producers’ access to foreign
markets, USDA should reverse its counterproductive policy of prohibiting private
companies from testing for BSE at their own expense. In the past, a private
company sought permission to test animals for BSE at their own facility, using
the same test that USDA employs to detect BSE, in order to be able to export
beef to Japan, which requires testing of all animals over 20 months at
slaughter. However, USDA has prohibited sale of test kits for this purpose. In
an era of limited governmental resources, when public-private partnerships are
essential to assure safety, we urge USDA to reconsider this highly
counterproductive and anti-competitive policy.

USDA has argued that the rapid tests are “worthless” when used for a food
safety purpose because their use could result in a false negative.7 While we
agree the rapid test kits can miss a case of BSE in the early stages of
incubation, such test kits can catch the disease in later stages, before the
animals show symptoms.8 They are used to test animals at slaughter in Europe and
Japan and have identified more than 1,000 otherwise undetected cases in Europe.9
We urge USDA to allow private testing, with the caveat that any findings of a
BSE positive animal would have to be immediately reported to the USDA. Although
tested beef should not be labeled “BSE-free,” testing could in fact be
incentivized by allowing companies who use such tests to label their products as
"BSEtested." We would appreciate having an opportunity to discuss these
recommendations with you and your staff. Thank you for your consideration.

>>> The animal in question was 10 years and 7 months old I am
curious, maybe I missed it somewhere, but was there paperwork on this mad cow,
or was dental detention used to determine the age of the cattle ?

I remember one of the other USA mad cows had no paper work and officials
had to use dental detention to guess the age of that mad cow.

detention, in my opinion, is another way to get around regulations. just
throw away the paperwork, and officials then can just guesstimate the age of the
mad cow, thus fudging on age by a few months, thus being able to keep in the so
called safe zone i.e. barb or not.

so, I am just curious as to if dental detention had to be used in this 4th
mad cow case ???

On March 13, 2006, the U.S. Department of Agriculture (USDA) announced the
confirmation of bovine spongiform encephalopathy (BSE) in a cow in Alabama. The
newly confirmed case was identified in a non-ambulatory (downer) cow on a farm
in Alabama. The animal was euthanized by a local veterinarian and buried on the
farm. The age of the cow was estimated by examination of the dentition as
10-years-old. It had no ear tags or distinctive marks; the herd of origin could
not be identified despite an intense investigation (see Alabama BSE
Investigation, Final Epidemiology Report, May 2006). http://www.fsis.usda.gov/ofo/tsc/bse_information.htm

It is important to reiterate here, even though this animal did not enter
the food chain, the fact that the USA now finds mad cow disease in samplings of
1 in 40,000 is very disturbing, and to add the fact that it was an atypical
L-type BASE BSE, well that is very disturbing in itself. 1 out of 40,000, would
mean that there were around 25 mad cows in the USA annually going by a National
herd of 100 million (which now I don’t think the USA herd is that big), but then
you add all these disturbing factors together, the documented link of sporadic
CJD cases to atypical L-type BASE BSE, the rise in sporadic CJD cases in the USA
of a new strain of CJD called ‘classification pending Creutzfeldt Jakob Disease’
cpCJD, in young and old, with long duration of clinical symptoms until death.
the USA has a mad cow problem and have consistently covered it up. it’s called
the SSS policy. ...

so, USDA et al accidently find two atypical mad cows in Texas and Alabama
during the infamous enhanced BSE cover up back in 2004 and 2005, and then shut
the testing down to numbers so low, it’s almost impossible to find another mad
cow case, unless your country is to a point that mad cow disease can be found in
1 in 40,000, and STILL FIND MAD COW DISEASE. partial and voluntary BSE mad cow
feed ban of August 4, 1997 was nothing more than ink on paper, with as much as
10,000,000 LBS. of blood laced meat and bone meal MBM going out into commerce 10
years later in 2007. who knows since 2007 breach, fda et al stopped posting
those warning letters. ARS said if atypical BSE was more virulent, SRM removal
would have to change if tissue infectivity was found differently than c-BSE. it
was. more virulent and infectivity was found in more tissues, including skeletal
muscle. HOUSTON, WE HAVE A PROBLEM. ...

I am deeply disturbed about the false and terribly misleading information
that is being handed out by the USDA FDA et al about this recent case of the
atypical L-type BASE BSE case in California. these officials are terribly
misinformed (I was told they are not lying), about the risk factor and
transmissibility of the atypical L-type BASE BSE. along with the USDA et al, the
media is following through with these lies. these are very disturbing
transmission studies that the CDC PUT OUT IN 2012. I urge officials to come
forward with the rest of this story.

We report transmission of atypical L-type bovine spongiform encephalopathy
to mouse lemurs after oral or intracerebral inoculation with infected bovine
brain tissue. After neurologic symptoms appeared, transmissibility of the
disease by both inoculation routes was confirmed by detection of
disease-associated prion protein in samples of brain tissue.

snip...

Conclusions

We demonstrated that the agent of L-BSE can be transmitted by the oral
route from cattle to mouse lemurs. As expected, orally inoculated animals
survived longer than IC-inoculated animals. Orally inoculated lemurs had less
severe clinical signs and symptoms, with no evidence of motor dysfunction. It
was previously suggested that the agent of L-BSE might be involved in the
foodborne transmission of a prion disease in mink (11,12), a species in which
several outbreaks of transmissible mink encephalopathy had been identified,
notably in the United States (13).

Our study clearly confirms, experimentally, the potential risk for
interspecies oral transmission of the agent of L-BSE. In our model, this risk
appears higher than that for the agent of classical BSE, which could only be
transmitted to mouse lemurs after a first passage in macaques (14). We report
oral transmission of the L-BSE agent in young and adult primates. Transmission
by the IC route has also been reported in young macaques (6,7). A previous study
of L-BSE in transgenic mice expressing human PrP suggested an absence of any
transmission barrier between cattle and humans for this particular strain of the
agent of BSE, in contrast to findings for the agent of classical BSE (9). Thus,
it is imperative to maintain measures that prevent the entry of tissues from
cattle possibly infected with the agent of L-BSE into the food chain.

Background: Three BSE types (classical and two atypical) have been
identified on the basis of molecular characteristics of the misfolded protein
associated with the disease. To date, each of these three types have been
detected in Canadian cattle.

Objectives: This study was conducted to further characterize the 16
Canadian BSE cases based on the biochemical properties of there associated
PrPres. Methods: Immuno-reactivity, molecular weight, glycoform profiles and
relative proteinase K sensitivity of the PrPres from each of the 16 confirmed
Canadian BSE cases was determined using modified Western blot analysis.

Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type
and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and
changes in glycosylation similar to other atypical BSE cases. PK digestion under
mild and stringent conditions revealed a reduced protease resistance of the
atypical cases compared to the C-type cases. N terminal- specific antibodies
bound to PrPres from H type but not from C or L type. The C-terminal-specific
antibodies resulted in a shift in the glycoform profile and detected a fourth
band in the Canadian H-type BSE.

Discussion: The C, L and H type BSE cases in Canada exhibit molecular
characteristics similar to those described for classical and atypical BSE cases
from Europe and Japan. This supports the theory that the importation of BSE
contaminated feedstuff is the source of C-type BSE in Canada. *** It also
suggests a similar cause or source for atypical BSE in these countries.

Human variant Creutzfeldt-Jakob Disease (vCJD) results from foodborne
transmission of prions from slaughtered cattle with classical Bovine Spongiform
Encephalopathy (cBSE). Atypical forms of BSE, which remain mostly asymptomatic
in aging cattle, were recently identified at slaughterhouses throughout Europe
and North America, raising a question about human susceptibility to these new
prion strains.

Methodology/Principal Findings

Brain homogenates from cattle with classical BSE and atypical (BASE)
infections were inoculated intracerebrally into cynomolgus monkeys (Macacca
fascicularis), a non-human primate model previously demonstrated to be
susceptible to the original strain of cBSE. The resulting diseases were compared
in terms of clinical signs, histology and biochemistry of the abnormal prion
protein (PrPres). The single monkey infected with BASE had a shorter survival,
and a different clinical evolution, histopathology, and prion protein (PrPres)
pattern than was observed for either classical BSE or vCJD-inoculated animals.
Also, the biochemical signature of PrPres in the BASE-inoculated animal was
found to have a higher proteinase K sensitivity of the octa-repeat region. We
found the same biochemical signature in three of four human patients with
sporadic CJD and an MM type 2 PrP genotype who lived in the same country as the
infected bovine.

Conclusion/Significance

Our results point to a possibly higher degree of pathogenicity of BASE
than classical BSE in primates and also raise a question about a possible link
to one uncommon subset of cases of apparently sporadic CJD. Thus, despite the
waning epidemic of classical BSE, the occurrence of atypical strains should
temper the urge to relax measures currently in place to protect public health
from accidental contamination by BSE-contaminated products.

Funding: This work has been supported by the Network of Excellence
NeuroPrion.

Competing interests: CEA owns a patent covering the BSE diagnostic tests
commercialized by the company Bio-Rad.

* E-mail: emmanuel.comoy@cea.fr

snip...

In summary, we have transmitted one atypical form of BSE (BASE) to a
cynomolgus macaque monkey that had a shorter incubation period than monkeys
infected with classical BSE, with distinctive clinical, neuropathological, and
biochemical features; and have shown that the molecular biological signature
resembled that seen in a comparatively uncommon subtype of sporadic CJD. We
cannot yet say whether BASE is more pathogenic for primates (including humans)
than cBSE, nor can we predict whether its molecular biological features
represent a clue to one cause of apparently sporadic human CJD. However, the
evidence presented here and by others justifies concern about a potential human
health hazard from undetected atypical forms of BSE, and despite the waning
epizoonosis of classical BSE, it would be premature to abandon the precautionary
measures that have been so successful in reversing the impact of cBSE. We would
instead urge a gradual, staged reduction that takes into account the evolving
knowledge about atypical ruminant diseases, and both a permanent ban on the use
of bovine central nervous system tissue for either animal or human use, and its
destruction so as to eliminate any risk of environmental contamination.

To date the OIE/WAHO assumes that the human and animal health standards
set out in the BSE chapter for classical BSE (C-Type) applies to all forms of
BSE which include the H-type and L-type atypical forms. This assumption is
scientifically not completely justified and accumulating evidence suggests that
this may in fact not be the case. Molecular characterization and the spatial
distribution pattern of histopathologic lesions and immunohistochemistry (IHC)
signals are used to identify and characterize atypical BSE. Both the L-type and
H-type atypical cases display significant differences in the conformation and
spatial accumulation of the disease associated prion protein (PrPSc) in brains
of afflicted cattle. Transmission studies in bovine transgenic and wild type
mouse models support that the atypical BSE types might be unique strains because
they have different incubation times and lesion profiles when compared to C-type
BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian
hamster the resulting molecular fingerprint had changed, either in the first or
a subsequent passage, from L-type into C-type BSE. In addition, non-human
primates are specifically susceptible for atypical BSE as demonstrated by an
approximately 50% shortened incubation time for L-type BSE as compared to
C-type. Considering the current scientific information available, it cannot be
assumed that these different BSE types pose the same human health risks as
C-type BSE or that these risks are mitigated by the same protective measures.

This study will contribute to a correct definition of specified risk
material (SRM) in atypical BSE. The incumbent of this position will develop new
and transfer existing, ultra-sensitive methods for the detection of atypical BSE
in tissue of experimentally infected cattle.

The TSE road map defining the evolution of European policy for protection
against prion diseases is based on a certain numbers of hypotheses some of which
may turn out to be erroneous. In particular, a form of BSE (called atypical
Bovine Spongiform Encephalopathy), recently identified by systematic testing in
aged cattle without clinical signs, may be the origin of classical BSE and thus
potentially constitute a reservoir, which may be impossible to eradicate if a
sporadic origin is confirmed.

***Also, a link is suspected between atypical BSE and some apparently
sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases
constitute an unforeseen first threat that could sharply modify the European
approach to prion diseases.

Background: BASE is an atypical form of bovine spongiform encephalopathy
caused by a prion strain distinct from that of BSE. Upon experimental
transmission to cattle, BASE induces a previously unrecognized disease phenotype
marked by mental dullness and progressive atrophy of hind limb musculature.
Whether affected muscles contain infectivity is unknown. This is a critical
issue since the BASE strain is readily transmissible to a variety of hosts
including primates, suggesting that humans may be susceptible.

Objectives: To investigate the distribution of infectivity in peripheral
tissues of cattle experimentally infected with BASE. Methods: Groups of Tg mice
expressing bovine PrP (Tgbov XV, n= 7-15/group) were inoculated both i.c. and
i.p. with 10% homogenates of a variety of tissues including brain, spleen,
cervical lymph node, kidney and skeletal muscle (m. longissimus dorsi) from
cattle intracerebrally infected with BASE. No PrPres was detectable in the
peripheral tissues used for inoculation either by immunohistochemistry or
Western blot.

Results: Mice inoculated with BASE-brain homogenates showed clinical signs
of disease with incubation and survival times of 175±15 and 207±12 days. Five
out of seven mice challenged with skeletal muscle developed a similar
neurological disorder, with incubation and survival times of 380±11 and 410±12
days. At present (700 days after inoculation) mice challenged with the other
peripheral tissues are still healthy. The neuropathological phenotype and PrPres
type of the affected mice inoculated either with brain or muscle were
indistinguishable and matched those of Tgbov XV mice infected with natural BASE.

Discussion: Our data indicate that the skeletal muscle of cattle
experimentally infected with BASE contains significant amount of infectivity, at
variance with BSE-affected cattle, raising the issue of intraspecies
transmission and the potential risk for humans. Experiments are in progress to
assess the presence of infectivity in skeletal muscles of natural BASE.

LET’S see how that mad cow triple firewall aka mad cow feed ban is working
out $$$

*** BANNED MAD COW FEED IN THE USA IN COMMERCE TONS AND TONS

THIS is just ONE month report, of TWO recalls of prohibited banned MBM,
which is illegal, mixed with 85% blood meal, which is still legal, but yet we
know the TSE/BSE agent will transmit blood. we have this l-BSE in North America
that is much more virulent and there is much concern with blood issue and l-BSE
as there is with nvCJD in humans. some are even starting to be concerned with
sporadic CJD and blood, and there are studies showing transmission there as
well. ... this is one month recall page, where 10 MILLION POUNDS OF BANNED MAD
COW FEED WENT OUT INTO COMMERCE, TO BE FED OUT. very little of the product that
reaches commerce is ever returned via recall, very, very little. this was 2007,
TEN YEARS AFTER THE AUGUST 4, 1997, PARTIAL AND VOLUNTARY MAD COW FEED BAN IN
THE USA, that was nothing but ink on paper. i have listed the tonnage of mad cow
feed that was in ALABAMA in one of the links too, this is where the infamous
g-h-BSEalabama case was, a genetic relation matching the new sporadic CJD in the
USA. seems this saga just keeps getting better and better.......$$$

Blood meal used to make cattle feed was recalled because it was cross-
contaminated with prohibited bovine meat and bone meal that had been
manufactured on common equipment and labeling did not bear cautionary BSE
statement.

Americans might remember that when the first mad cow was confirmed in the
United States in December, 2003, it was major news. The United States Department
of Agriculture (USDA) and the Food and Drug Administration (FDA) had been
petitioned for years by lawyers from farm and consumer groups I worked with to
stop the cannibal feeding practices that transmit this horrible, always fatal,
human and animal dementia. When the first cow was found in Washington state, the
government said it would stop such feeding, and the media went away. But once
the cameras were off and the reporters were gone nothing substantial changed.

In the United States, dairy calves are still taken from their mothers and
fed the blood and fat of dead cattle. This is no doubt a way to infect them with
the mad cow disease that has now been incubating here for decades, spread
through such animal feeding practices. No one knows how the latest dairy cow was
infected, the fourth confirmed in the United States. Maybe it was nursed on
cow's blood. Perhaps it was fed feed containing cattle fat with traces of cattle
protein. Or perhaps there is a mad cow disease in pigs in the United States,
which simply has not been found yet, because pigs are not tested for it at all,
even though pigs are fed both pig and cattle byproducts, and then the blood, fat
and other waste parts of these pigs are fed to cattle.

All these U.S. cattle feeding methods are long banned and illegal in other
countries that suffered through but eventually dealt properly with mad cow
disease. Here, rather than stopping the transmission of the disease by stopping
the cannibal feeding, mad cow is simply covered up with inadequate testing and
very adequate public relations. US cattle are still fed mammalian blood, fat and
protein, risking human deaths and threatening the long term safety of human
blood products, simply to provide the U.S. livestock industry with a cheap
protein source and a cheap way to get rid of dead animal waste.

I began researching this issue around 1989, long before the disease was
confirmed to have jumped from cattle to the people eating them, as announced by
the British government in 1996. In 1997 I co-authored <http://www.prwatch.org/books/madcow.html>
Mad Cow USA, warning that the disease was likely already here and spreading,
since the animal cannibalism that caused its outbreak in Britain and spread it
to other countries was actually more widespread in the United States than
anywhere.

Some years ago responsible U.S. beef companies wanted to test their
animals for mad cow disease and label their beef as being disease free, but they
were forbidden under penalty of law from doing so. Only the USDA can test for
mad cows in America. In 2004 and 2005, after two additional mad cows were
discovered in Texas and Alabama, the United Sates government declared that
obviously mad cow wasn't much of a problem and gutted it's anemic testing
program. Today only about 40,000 cattle a year are tested, out of tens of
millions slaughtered. It's amazing that the California cow was even detected
given this pathetic testing program that seems well designed to hide rather than
find mad cows.

The prevention of mad cow disease is relatively simple. If your country
has it, test each animal before it goes to slaughter to keep the diseased
animals out of the food chain. Cheap, accurate and easy tests are now available
in other countries but illegal here. Testing cattle both identifies the true
extent of the disease, and keeps infected animals from being eaten in your
sausage or hamburger. In this manner countries like Britain, Germany, France and
Japan have controlled their problem through testing and a strict ban on cannibal
feed.

Once mad cow disease moves into the human population of a country, all
bets are off as to what could happen next. It's a very slow disease, it develops
invisibly over decades in someone who has been infected, and it is always fatal.
We'll know a lot more in fifty years, but the future looks worrisome. In Britain
people are dying from mad cow disease, people who never consumed infected meat.
They used medical products containing human blood, and that blood was infected
because it was from infected people. There is no test to identify infectious
prions, the causal agent, in blood.

Almost none of this information appeared in news stories about the
California mad cow. Instead the headlines and the talking heads fed us the line
that the United States fixed this problem long ago, and the fact that only 4 mad
cows have been detected so far is proof of our success. Oprah Winfrey once tried
via her talk show to warn about this, way back in 1996, but Texas cattlemen
dragged her and her guest Howard Lyman into court and she had to spend many
millions of dollars defending herself from the supposed crime of slandering
meat.

Oprah won her case, which was probably unfortunate for the rest of us
because had she been convicted the ensuing appeals court trial might have gotten
enough attention to wake up Americans to the truth. Instead Oprah learned her
lesson - shut up and you won't get sued. Other media learned too that if the
government and industry can silence Oprah, they can muzzle anyone. (One of the 4
confirmed U.S. mad cows was later found in Texas, appropriately enough.)

There are a handful of dedicated activists such as Howard Lyman who have
been sounding the alarm on this. They include the ecologist Dr. Michael Hansen
of Consumers Union and Dr. Michael Greger, a physician. Terry Singeltary Sr.,
whose mom died of a version of the human form of mad cow disease, has been a
relentless, unpaid activist on this issue.

Despite their dedicated work, there is no indication that anything is
going to change here in America. The U.S. government refuses to implement the
feed ban and the animal testing necessary. It doesn't matter if the President is
named Clinton, Bush or Obama because their bureaucrats in the USDA and FDA stay
the course and keep the cover up going. Docile, eating what they are fed,
trusting the rancher all the way to the slaughterhouse. Is that just the cows,
or is it us too?

In order to stop the spread of bovine spongiform encephalopathy (BSE or
mad cow disease), the US Department of Agriculture should adopt and enforce the
same strict standards required by the European Union and Japan:

* Mandatory testing for all cattle brought to slaughter, before they enter
the food chain.

* Ban the feeding of blood, manure, and slaughterhouse waste to animals.

In the meantime, the USDA must stop harassing farmers and food processors
who are interested in independently testing their own beef for mad cow disease.

Ironically, the news that mad cow is still in our food supply comes at a
time that the U.S. Department of Agriculture Animal and Plant Health Inspection
Service (APHIS) is proposing to drop significant protections the U.S. has
against the importation of cattle infected with mad cow disease.

APHIS proposes to open United States' borders to cattle from countries
that have had thousands of cases of BSE, and where new BSE cases continue to be
found. The importation of a single infected cow from Canada in 2001 set in
motion restrictions on U.S. beef exports that cost the beef industry billions of
dollars and that still exist today in several major export markets.

APHIS also proposes to drop important measures that have been used to
protect U.S. consumers from these imported cattle and meat products (which have
a much higher chance of being infected with BSE than U.S.-raised cattle), and
intends to rely almost exclusively on slaughtering techniques, particularly the
removal of specified risk materials (SRMs), which we know on occasion is not
employed fully or effectively, and which has not been practiced long enough to
determine whether it is indeed the panacea APHIS assumes, given the long
gestation time of variant Creutzfeldt-Jakob Disease (vCJD) in humans.

I support the view of R-CALF USA CEO Bill Bullard:

"Seventy-six farm and consumer organizations, representing tens of
millions of U.S. citizens, recently urged Secretary Vilsack to strengthen, not
weaken, our already lax BSE policies by reversing the so-called
'over-thirty-month rule,' which allows Canadian cattle born during the time the
BSE agent was known to be circulating in Canada's feed system to be imported
into the United States.

"Secretary Vilsack has again ignored our concerns and is putting the
self-interests of corporate meatpackers that want access to more meat supplies
regardless of risk to humans and livestock, ahead of the health and safety
concerns of U.S. citizens.

"The USDA is touting its proposed rule as a trade rule, claiming it will
strengthen the United States' negotiating position in trade agreements. This is
the same failed argument the Bush Administration used when it first relaxed our
U.S. BSE policies in 2004, and the result of that failed argument is that many
important export markets imposed long-lasting export restrictions on U.S. beef.

"USDA's proposal amounts to a unilateral disarmament of essential disease
protections for U.S. citizens and livestock. It will disadvantage U.S. producers
in the global market because other major beef exporters, including Brazil,
Australia, and India continue to maintain adequate import standards while the
U.S. relaxes its own. This will create unnecessary and avoidable anxieties among
other beef consuming nations for U.S. beef.

"Exposing U.S. consumers and U.S. livestock to a heightened risk of BSE
introduction is irresponsible and contrary to pledges made by the Obama
Administration during his campaign."

This is no time to relax our essential protections against the
introduction of mad cow disease.

so, USDA et al accidently find two atypical mad cows in Texas and Alabama
during the infamous enhanced BSE cover up back in 2004 and 2005, and then shut
the testing down to numbers so low, it's almost impossible to find another mad
cow case, unless your country is to a point that mad cow disease can be found in
1 in 40,000, and STILL FIND MAD COW DISEASE, HOUSTON, WE HAVE A PROBLEM. ...

PLEASE UNDERSTAND, the USDA et al are lying about atypical BSE being a
spontaneous mutation, NOT caused by feed. spontaneous BSE has NEVER been proven
in any natural field case of BSE. feed is the most likely route. ...tss

As previously stated most of the characteristics of atypical BSE have not
been defined. In addition to the origin, the risk to other cattle by means of
natural transmission, the risk to humans and other animal species suck as
chickens and pigs is still unknown as is the distribution of infectivity
throughout the body of a bovine. There is little information on clinical
manifestation if it occurs at all in certain of the cases. Documented L cases
have been diagnosed from samples taken from older ''healthy'' cattle presented
for routine slaughter.

While additional surveillance and research is being conducted, it is
important for policy make to consider the implications of atypical BSE. They may
need to rethink what populations are appropriate targets. It would probably be
unwise to prematurely lessen or discontinue the current BSE protection measures.

When atypical cases were first reported there was some speculation that
these may merely be protein accumulation disorders associated with old age. It
has now been shown that both the Land H types of atypical BSE are at least
experimentally transmissible. Homogenates from L cases have been transmitted to
bovinized transgenic mice, humanized transgenic mice, Cynomolgus monkeys and 1
breed of cattle (Buschmann et al. 2006; Book of abstracts (2006), International
Conference on Prion Diseases, Turin, Italy). H cases have been transmitted to
bovinized transgenic (Tgbov) and ovinized transgenic mice (Béringue et al.
2006). The incubation times for atypical L cases of BSE were shorter in the
Tgbov mice than classical BSE inoculated into Tgbov mice and the H cases had
longer incubations.

A variation or mutation of the classical BSE strain A different route
of exposure or exposure at an older age A strain of Scrapie transmitted to
cattle Sporadic or a spontaneous occurrence of BSE At his point in time,
there is no evidence to conclude that any of the theories are or are not a
possibility. There is considerable interest in the sporadic theory. If a form of
BSE were to ocnaturally, this may suggest that certain control and prevention
measure would have to remain in place indefinitely. Proving or disproving the
occurrence of a relatively rare sporadic disease poses a significant challenge.
It would require between 3 and 4.5 million tests performed on brain samples
randomly taken from cattle over 7 years of age in a country with no evidencrisk
from orally acquired BSE. It is unlikely that any country would have the will or
resources to perform such a study. Lacking this type of evidence, systematic
surveillance over a long time period may provide evidence about the nature of
atypical BSE.

When L-type BSE was inoculated into ovine transgenic mice and Syrian
hamster the resulting molecular fingerprint had changed, either in the first or
a subsequent passage, from L-type into C-type BSE. In addition, non-human
primates are specifically susceptible for atypical BSE as demonstrated by an
approximately 50% shortened incubation time for L-type BSE as compared to
C-type. Considering the current scientific information available, it cannot be
assumed that these different BSE types pose the same human health risks as
C-type BSE or that these risks are mitigated by the same protective measures.

This study will contribute to a correct definition of specified risk
material (SRM) in atypical BSE. The incumbent of this position will develop new
and transfer existing, ultra-sensitive methods for the detection of atypical BSE
in tissue of experimentally infected cattle.

Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October
31, 2005 INTRODUCTION The United States Department of Agriculture’s Food Safety
and Inspection Service (FSIS) held a public meeting on July 25, 2006 in
Washington, D.C. to present findings from the Harvard Risk Assessment of Bovine
Spongiform Encephalopathy Update, October 31, 2005 (report and model located on
the FSIS website:

> > > Ackerman says downed cattle are 50 times more likely to have
mad cow disease (also known as Bovine Spongiform Encephalopathy, or BSE) than
ambulatory cattle that are suspected of having BSE. Of the 20 confirmed cases of
mad cow disease in North America since 1993, at least 16 have involved downer
cattle, he said. < < <

don’t forget the children...

PLEASE be aware, for 4 years, the USDA fed our children all across the
Nation (including TEXAS) dead stock downer cows, the most high risk cattle for
BSE aka mad cow disease and other dangerous pathogens.

4.6.1. Epidemiology TME is a disease that affected mink ranches, decimating
the herds, in the frame of five to eleven isolated outbreaks, from 1947 to 1985,
mainly in USA (Wisconsin was the main affected State since it is where mink
ranches where mainly located) (Robinson et al., 1994). Moreover, eastern
European countries (East Germany, Finland and USSR) also reported outbreaks in
the mid-sixties.

According to its rare occurrence associated with a massive rate of
infection, and in the absence of probing horizontal or vertical transmission,
the hypothesis of a food-borne infection is the most convincing explanation.
This theory is enforced by the fact that three of those outbreaks occurred in
large mink production facilities that prepared on-site feed involving the use of
non-ambulatory (i.e. animal unable to stand alone) cattle (Hartsoug and Burger,
1965; Marsh et al.,

In April of 1985, a mink rancher in Wisconsin reported a debilitating
neurologic disease in his herd which we diagnosed as TME by histopathologic
findings confirmed by experimental transmission to mink and squirrel monkeys.
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead
dairy cattle and a few horses. She had never been fed.

We believe that these findings may indicate the presence of a previously
unrecognized scrapie-like disease in cattle and wish to alert dairy
practitioners to this possibility.

snip...

PROCEEDINGS OF THE SEVENTH ANNUAL WESTERN CONFERENCE FOR FOOD ANIMAL
VETERINARY MEDICINE, University of Arizona, March 17-19, 1986

Transmissible mink encepholapathy (TME) is a foodborne transmissible
spongiform encephalopathy (TSE) of ranch-raised mink; infection with a ruminant
TSE has been proposed as the cause, but the precise origin of TME is unknown. To
compare the phenotypes of each TSE, bovine-passaged TME isolate and 3 distinct
natural bovine spongiform encephalopathy (BSE) agents (typical BSE, H-type BSE,
and L-type BSE) were inoculated into an ovine transgenic mouse line (TgOvPrP4).
Transgenic mice were susceptible to infection with bovine-passaged TME, typical
BSE, and L-type BSE but not to H-type BSE. Based on survival periods, brain
lesions profiles, disease-associated prion protein brain distribution, and
biochemical properties of protease-resistant prion protein, typical BSE had a
distint phenotype in ovine transgenic mice compared to L-type BSE and bovine
TME.The similar phenotypic properties of L-type BSE and bovine TME in TgOvPrP4
mice suggest that L-type BSE is a much more likely candidate for the origin of
TME than is typical BSE.

snip...

Conclusion

These studies provide experimental evidence that the Stetsonville TME
agent is distinct from typical BSE but has phenotypic similarities to L-type BSE
in TgOvPrP4 mice. Our conclusion is that L-type BSE is a more likely candidate
for a bovine source of TME infection than typical BSE. In the scenario that a
ruminant TSE is the source for TME infection in mink, this would be a second
example of transmission of a TSE from ruminants to non-ruminants under natural
conditions or farming practices in addition to transmission of typical BSE to
humans, domestic cats, and exotic zoo animals(37). The potential importance of
this finding is relevant to L-type BSE, which based on experimental transmission
into humanized PrP transgenic mice and macaques, suggests that L-type BSE is
more pathogenic for humans than typical BSE (24,38).

The epidemiology of Transmissible mink encephalopathy (TME) indicates an
alimentary origin. Several inter-species transmission experiments have not
succeeded in establishing with certainty any natural reservoir of this prion
strain, although both ovine and bovine sources have been suspected. Cattle
exposed to TME develop a spongiform encephalopathy that is distinct from
classical Bovine Spongiform Encephalopathy (c-BSE).

Inoculation of c-BSE to cynomolgus macaque provided early evidence of a
possible risk to humans, and remains an important model to define the risk of
both primary (oral transmission from cattle to primate) and secondary
(intravenous intra-species transmission) exposures. We have also evaluated the
transmissibility of other cattle prion strains to macaques, including L- and H-
atypical forms of BSE, namely BSE-L and BSE-H, and cattle-adapted TME.

BSE-L induced a neurological disease distinct from c-BSE. Peripheral
exposures demonstrate the transmissibility of BSE-L by oral, intravenous, and
intra-cerebral routes, with incubation periods similar to c-BSE. Cattle-adapted
TME also induced a rapid disease in cynomolgus macaque. The clinical features,
lesion profile, and biochemical signature of the induced disease was similar to
the features observed in animals exposed to BSE-L, suggesting a link between the
two prion strains. Secondary transmissions to a common host (transgenic mouse
overexpressing bovine PrP) of cattle-TME and BSE-L before or after passage in
primates induced diseases with similar incubation periods: like the c-BSE
strain, these cattle strains maintained their distinctive features regardless of
the donor species and passages.

If the link between TME and BSE-L is confirmed, our results would suggest
that BSE-L in North America may have existed for decades, and highlight a
possible preferential transmission of animal prion strains to primates after
passage in cattle.

1. Dr Clark lately of the Scrapie Research Unit, Mission Texas has
successfully transmitted ovine and caprine scrapie to cattle. The experimental
results have not been published but there are plans to do this. This work was
initiated in 1978. A summary of it is:-

Expt A 6 Her x Jer calves born in 1978 were inoculated as follows with a
2nd Suffolk scrapie passage:-

i/c 1ml i/m, 5ml; s/c 5ml; oral 30ml.

1/6 went down after 48 months with a scrapie/BSE-like disease.

Expt B 6 Her or Jer or HxJ calves were inoculated with angora Goat virus
2/6 went down similarly after 36 months.

Expt C Mice inoculated from brains of calves/cattle in expts A & B
were resistant, only 1/20 going down with scrapie and this was the reason given
for not publishing.

Diagnosis in A, B, C was by histopath. No reports on SAF were given.

Dr Warren Foote indicated success so far in eliminating scrapie in
offspring from experimentally- (and naturally) infected sheep by ET. He had
found difficulty in obtaining emhryos from naturally infected sheep (cf SPA).

3. Prof. A Robertson gave a brief account of BSE. The US approach was to

PAGE 32

accord it a very low profile indeed. Dr A Thiermann showed the picture in
the "Independent" with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. BSE was not reported in USA.

4. Scrapie incidents (ie affected flocks) have shown a dramatic increase
since 1978. In 1953 when the National Control Scheme was started there were
10-14 incidents, in 1978 - 1 and in 1988 so far 60.

5. Scrapie agent was reported to have been isolated from a solitary fetus.

6. A western blotting diagnostic technique (? on PrP} shows some promise.

7. Results of a questionnaire sent to 33 states on the subject of the
national sheep scrapie programme survey indicated;

17/33 wished to drop it 6/33 wished to develop it 8/33 had few sheep and
were neutral

Information obtained from Dr Wrathall's notes of a meeting of the U.S.
Animal Health Association at Little Rock, Arkansas Nov. 1988.

Long-term effects of CWD on cervid populations and ecosystems remain
unclear as the disease continues to spread and prevalence increases. In captive
herds, CWD might persist at high levels and lead to complete herd destruction in
the absence of human culling. Epidemiologic modeling suggests the disease could
have severe effects on free-ranging deer populations, depending on hunting
policies and environmental persistence (8,9). CWD has been associated with large
decreases in free-ranging mule deer populations in an area of high CWD
prevalence (Boulder, Colorado, USA) (5).

SNIP...

Reasons for Caution There are several reasons for caution with respect to
zoonotic and interspecies CWD transmission. First, there is strong evidence that
distinct CWD strains exist (36). Prion strains are distinguished by varied
incubation periods, clinical symptoms, PrPSc conformations, and CNS PrPSc
depositions (3,32). Strains have been identified in other natural prion
diseases, including scrapie, BSE, and CJD (3). Intraspecies and interspecies
transmission of prions from CWD-positive deer and elk isolates resulted in
identification of >2 strains of CWD in rodent models (36), indicating that
CWD strains likely exist in cervids. However, nothing is currently known about
natural distribution and prevalence of CWD strains. Currently, host range and
pathogenicity vary with prion strain (28,37). Therefore, zoonotic potential of
CWD may also vary with CWD strain. In addition, diversity in host (cervid) and
target (e.g., human) genotypes further complicates definitive findings of
zoonotic and interspecies transmission potentials of CWD. Intraspecies and
interspecies passage of the CWD agent may also increase the risk for zoonotic
CWD transmission. The CWD prion agent is undergoing serial passage naturally as
the disease continues to emerge. In vitro and in vivo intraspecies transmission
of the CWD agent yields PrPSc with an increased capacity to convert human PrPc
to PrPSc (30). Interspecies prion transmission can alter CWD host range (38) and
yield multiple novel prion strains (3,28). The potential for interspecies CWD
transmission (by cohabitating mammals) will only increase as the disease spreads
and CWD prions continue to be shed into the environment. This environmental
passage itself may alter CWD prions or exert selective pressures on CWD strain
mixtures by interactions with soil, which are known to vary with prion strain
(25), or exposure to environmental or gut degradation. Given that prion disease
in humans can be difficult to diagnose and the asymptomatic incubation period
can last decades, continued research, epidemiologic surveillance, and caution in
handling risky material remain prudent as CWD continues to spread and the
opportunity for interspecies transmission increases. Otherwise, similar to what
occurred in the United Kingdom after detection of variant CJD and its subsequent
link to BSE, years of prevention could be lost if zoonotic transmission of CWD
is subsequently identified, SNIP...SEE FULL TEXT ;

Thank you for your recent letter concerning the publication of the third
annual report from the CJD Surveillance Unit. I am sorry that you are
dissatisfied with the way in which this report was published.

The Surveillance Unit is a completely independant outside body and the
Department of Health is committed to publishing their reports as soon as they
become available. In the circumstances it is not the practice to circulate the
report for comment since the findings of the report would not be amended. In
future we can ensure that the British Deer Farmers Association receives a copy
of the report in advance of publication.

The Chief Medical Officer has undertaken to keep the public fully informed
of the results of any research in respect of CJD. This report was entirely the
work of the unit and was produced completely independantly of the the
Department.

The statistical results reqarding the consumption of venison was put into
perspective in the body of the report and was not mentioned at all in the press
release. Media attention regarding this report was low key but gave a realistic
presentation of the statistical findings of the Unit. This approach to
publication was successful in that consumption of venison was highlighted only
once by the media ie. in the News at one television proqramme.

I believe that a further statement about the report, or indeed statistical
links between CJD and consumption of venison, would increase, and quite possibly
give damaging credence, to the whole issue. From the low key media reports of
which I am aware it seems unlikely that venison consumption will suffer
adversely, if at all.

Consumption of venison and veal was much less widespread among both cases
and controls. For both of these meats, there was evidence of a trend with
increasing frequency of consumption being associated with increasing risk of
CJD. These associations were largely unchanged when attention was restricted to
pairs with data obtained from relatives. ...

O.K. let's compare some recent cases of this prionpathy in other countries
besides Gambetti's first 10 recently, that he claims is a spontaneous event,
from a genetic disorder, that is not genetic, but sporadic, that is related to
no animal TSE in North America, or the world. ...

How the California cow got the disease remains unknown. Government
officials expressed confidence that contaminated food was not the source, saying
the animal had atypical L-type BSE, a rare variant not generally associated with
an animal consuming infected feed.

However, a BSE expert said that consumption of infected material is the
only known way that cattle get the disease under natural conditons.

“In view of what we know about BSE after almost 20 years experience,
contaminated feed has been the source of the epidemic,” said Paul Brown, a
scientist retired from the National Institute of Neurological Diseases and
Stroke.

BSE is not caused by a microbe. It is caused by the misfolding of the
so-called “prion protein” that is a normal constituent of brain and other
tissues. If a diseased version of the protein enters the brain somehow, it can
slowly cause all the normal versions to become misfolded.

It is possible the disease could arise spontaneously, though such an event
has never been recorded, Brown said.

In a statement released on 24 April, Karen Ross, Secretary of the
California Department of Food and Agriculture said, “The detection of BSE shows
that the surveillance program in place in California and around the country is
working.” Food safety advocates such as Yonkers, New York, -based Consumers
Union say it’s a warning sign that surveillance is inadequate and needs to be
stepped up.

Ross’s statement also makes a point of noting a key feature of this
particular case: The infected cow carried what is known as ‘L-type’ BSE, a
version of the disease that has not been detected before in the US and has so
far not been associated with transmission through animal feed. As the policy
debate over testing rumbles on, here is a short guide to what is known and not
known about this rare strain and its unexpected appearance.

SACRAMENTO, April 24, 2012 – CDFA Secretary Karen Ross issued this
statement following the USDA’s announcement of the detection of atypical bovine
spongiform encephalopathy (BSE) in a California dairy cow:

“The detection of BSE shows that the surveillance program in place in
California and around the country is working. Milk and beef remain safe to
consume. The disease is not transmitted through milk. Because of the strength of
the food protection system, the cow did not enter the food or feed supply. There
are numerous safeguards in place to prevent BSE from entering the food
chain.

“The atypical BSE designation is important because this is a very rare form
of BSE not generally associated with an animal consuming infected feed. CDFA
veterinarians are working with the USDA to investigate this case and to identify
whether additional cows are at risk. Feed restrictions in place in California
and around the country for the last 15 years minimize that risk to the greatest
degree possible. We will provide additional information about this case as it
becomes available.”

In an article today for United Press International, science reporter Steve
Mitchell writes:

Analysis: What that mad cow means

By STEVE MITCHELL UPI Senior Medical Correspondent

WASHINGTON, March 15 (UPI) -- The U.S. Department of Agriculture was quick
to assure the public earlier this week that the third case of mad cow disease
did not pose a risk to them, but what federal officials have not acknowledged is
that this latest case indicates the deadly disease has been circulating in U.S.
herds for at least a decade.

The second case, which was detected last year in a Texas cow and which
USDA officials were reluctant to verify, was approximately 12 years old.

These two cases (the latest was detected in an Alabama cow) present a
picture of the disease having been here for 10 years or so, since it is thought
that cows usually contract the disease from contaminated feed they consume as
calves. The concern is that humans can contract a fatal, incurable,
brain-wasting illness from consuming beef products contaminated with the mad cow
pathogen.

"The fact the Texas cow showed up fairly clearly implied the existence of
other undetected cases," Dr. Paul Brown, former medical director of the National
Institutes of Health's Laboratory for Central Nervous System Studies and an
expert on mad cow-like diseases, told United Press International. "The question
was, 'How many?' and we still can't answer that."

Brown, who is preparing a scientific paper based on the latest two mad cow
cases to estimate the maximum number of infected cows that occurred in the
United States, said he has "absolutely no confidence in USDA tests before one
year ago" because of the agency's reluctance to retest the Texas cow that
initially tested positive.

USDA officials finally retested the cow and confirmed it was infected
seven months later, but only at the insistence of the agency's inspector
general.

"Everything they did on the Texas cow makes everything they did before
2005 suspect," Brown said.

Despite this, Brown said the U.S. prevalence of mad cow, formally known as
bovine spongiform encephalopathy, or BSE, did not significantly threaten human
or cattle health.

"Overall, my view is BSE is highly unlikely to pose any important risk
either in cattle feed or human feed," he said.

However, Jean Halloran of Consumers Union in Yonkers, N.Y., said consumers
should be troubled by the USDA's secrecy and its apparent plan to dramatically
cut back the number of mad cow tests it conducts.

"Consumers should be very concerned about how little we know about the
USDA's surveillance program and the failure of the USDA to reveal really
important details," Halloran told UPI. "Consumers have to be really concerned if
they're going to cut back the program," she added.

Last year the USDA tested more than 300,000 animals for the disease, but
it has proposed, even in light of a third case, scaling back the program to
40,000 tests annually.

"They seem to be, in terms of actions and policies, taking a lot more
seriously the concerns of the cattle industry than the concerns of consumers,"
Halloran said. "It's really hard to know what it takes to get this
administration to take action to protect the public."

The USDA has insisted that the safeguards of a ban on incorporating cow
tissue into cattle feed (which is thought to spread the disease) and removal of
the most infectious parts of cows, such as the brain and spinal cord, protect
consumers. But the agency glosses over the fact that both of these systems have
been revealed to be inadequately implemented.

The feed ban, which is enforced by the Food and Drug Administration, has
been criticized by the Government Accountability Office in two reports, the most
recent coming just last year. The GAO said the FDA's enforcement of the ban
continues to have weaknesses that "undermine the nation's firewall against BSE."

USDA documents released last year showed more than 1,000 violations of the
regulations requiring the removal of brains and spinal cords in at least 35
states, Puerto Rico and the Virgin Islands, with some plants being cited
repeatedly for infractions. In addition, a violation of similar regulations that
apply to beef exported to Japan is the reason why Japan closed its borders to
U.S. beef in January six weeks after reopening them.

Other experts also question the adequacy of the USDA's surveillance
system. The USDA insists the prevalence of mad cow disease is low, but the
agency has provided few details of its surveillance program, making it difficult
for outside experts to know if the agency's monitoring plan is sufficient.

"It's impossible to judge the adequacy of the surveillance system without
having a breakdown of the tested population by age and risk status," Elizabeth
Mumford, a veterinarian and BSE expert at Safe Food Solutions in Bern,
Switzerland, a company that provides advice on reducing mad cow risk to industry
and governments, told UPI.

"Everybody would be happier and more confident and in a sense it might be
able to go away a little bit for (the USDA) if they would just publish a
breakdown on the tests," Mumford added.

UPI requested detailed records about animals tested under the USDA's
surveillance plan via the Freedom of Information Act in May 2004 but nearly two
years later has not received any corresponding documents from the agency,
despite a federal law requiring agencies to comply within 30 days. This leaves
open the question of whether the USDA is withholding the information, does not
have the information or is so haphazardly organized that it cannot locate it.

Mumford said the prevalence of the disease in U.S. herds is probably quite
low, but there have probably been other cases that have so far gone undetected.
"They're only finding a very small fraction of that low prevalence," she said.

Mumford expressed surprise at the lack of concern about the deadly disease
from American consumers. "I would expect the U.S. public to be more concerned,"
she said.

Markus Moser, a molecular biologist and chief executive officer of
Prionics, a Swiss firm that manufactures BSE test kits, told UPI one concern is
that if people are infected, the mad cow pathogen could become "humanized" or
more easily transmitted from person to person.

"Transmission would be much easier, through all kinds of medical
procedures" and even through the blood supply, Moser said.

"Actually, Terry, I have been critical of the USDA handling of the mad cow
issue for some years, and with Linda Detwiler and others sent lengthy detailed
critiques and recommendations to both the USDA and the Canadian Food Agency."

I am deeply disturbed about the false and terribly misleading information
that is being handed out by the USDA FDA et al about this recent case of the
atypical L-type BASE BSE case in California. these officials are terribly
misinformed (I was told they are not lying), about the risk factor and
transmissibility of the atypical L-type BASE BSE. these are very disturbing
transmission studies that the CDC PUT OUT IN 2012. I urge officials to come
forward with the rest of this story.

It is important to reiterate here, even though this animal did not enter
the food chain, the fact that the USA now finds mad cow disease in samplings of
1 in 40,000 is very disturbing, and to add the fact that it was an atypical
L-type BASE BSE, well that is very disturbing in itself. 1 out of 40,000, would
mean that there were around 25 mad cows in the USA annually going by a National
herd of 100 million (which now I don’t think the USA herd is that big), but then
you add all these disturbing factors together, the documented link of sporadic
CJD cases to atypical L-type BASE BSE, the rise in sporadic CJD cases in the USA
of a new strain of CJD called ‘classification pending Creutzfeldt Jakob Disease’
cpCJD, in young and old, with long duration of clinical symptoms until death.
the USA has a mad cow problem and have consistently covered it up. it’s called
the SSS policy. ...

see full text with updated transmission studies and science on the atypical
L-type BASE BSE Jan. 2012 CDC. ...